| 1. |
- Bennermo, Marie, et al.
(författare)
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Genetic and environmental influences on the plasma interleukin-6 concentration in patients with a recent myocardial infarction : a case-control study
- 2011
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Ingår i: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 31:2, s. 259-264
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Tidskriftsartikel (refereegranskat)abstract
- The aim was to study the stimuli responsible for triggering and sustaining the plasma concentration of the inflammatory marker interleukin-6 (IL-6) in patients with a first myocardial infarction before the age of 60 and healthy control subjects matched for age and sex. The plasma IL-6 concentration, antibodies against Chlamydia pneumoniae, cytomegalovirus, Epstein-Barr virus, Helicobacter pylori, herpes simplex type 1 and 2, and genotype for the IL6-174 G>C single-nucleotide polymorphism were determined 3 months after the acute event. The results showed that patients had higher IL-6 levels than control subjects, whereas there were no differences regarding individual or total number (pathogen burden) of positive antibody tests against the different pathogens or IL6 genotype distribution. The plasma IL-6 concentration was associated with the number of positive antibody tests in patients and control subjects, whereas patients irrespective of IL6 genotype had increased IL-6. Multivariate analysis, including traditional coronary heart disease risk factors, antibodies against pathogens, and IL6 genotype, explained 17% of the variation of the plasma IL-6 concentration. Neither pathogen burden nor IL6 genotype did contribute to the variation of plasma IL-6 levels, whereas smoking, body-mass index, hypertension, case-control status, and age were determinants of the plasma IL-6 concentration.
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| 2. |
- Björnstedt Bennermo, Marie
(författare)
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On the genetic variation of interleukin-6 in health and coronary heart disease
- 2005
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- There is increasing evidence that inflammation plays an important role in the development of atherosclerosis and coronary heart disease (CHD). Prospective studies on healthy individuals and on patients with unstable angina pectoris or non-Q-wave myocardial infarction have shown that individuals with high interleukin-6 (IL-6) concentrations have an increased risk of myocardial infarction and death due to cardiovascular disease. The mechanisms responsible for triggering and sustaining elevation of IL-6 in healthy subjects and patients with CHD are largely unknown and remain to be defined. Thrombosis underlies most of the acute manifestations of CHD including myocardial infarction. The causes of thrombosis are not fully clear, but an important mechanism might be the connection between inflammation and coagulation. The present research program was set up to investigate the genetic variation of IL-6 in vivo in health and CHD and connection between inflammation and coagulation. In study I 222 patients with ST-elevation myocardial infarction were included. They were genotyped for -174 G>C single nucleotide polymorphism (SNP) of the IL-6 gene. Plasma IL-6 concentration was measured at admission and after 48 hrs. This study showed that patients with IL-6 above the median at admission had an increased risk for CHD death or a new myocardial infarction, whereas the genotype did not influence CHD risk or plasma IL-6 levels. In study II and III, the effect of an inflammatory stimulus on circulating IL-6 and factor VIIa (FVlla) concentrations depending on genotype was investigated in forty healthy subjects by challenged vaccination with Salmonella typhii vaccine. The study subjects were genotyped for the -174 G>C SNP of the IL-6 gene and for the Arg353GIn SNP of the FVII gene. The result demonstrates that the response differed according to genotype, indicating that IL-6 and FVIIa are influenced by genetic variation. In study IV the influence of environmental factors and IL-6 genotype on IL-6 concentration was investigated. Three hundred eighty-seven patients with their first myocardial infarction before the age of 60 and matched healthy controls were enrolled. Antibodies against different pathogens were examined. Patients and controls were genotyped for the - 174 G>C SNP of the IL-6 gene. Plasma IL6 concentrations were significantly higher in patients compared to healthy controls when measured 3 months after the acute event. Furthermore, patients who were homozygous for the G-allele had higher IL-6 levels compared to those being hetereo- or homozygotes for the C-allele. In healthy controls no such genotype-phenotype association was found. We were not able to show any association between -174 G>C genotype and risk of CHD. Neither a single, nor a number of antibodies against multiple pathogens differed between patients and healthy controls and no associations between these and circulating IL-6 concentration were indicated. Conclusion: This thesis demonstrates that circulating IL-6 concentration is influenced by genetic variation of the IL-6 gene in vivo both in health and CHD. However, we found no association between the -174 G>C genotype of the IL-6 gene and CHD. Nonetheless, our results showed that patients with myocardial infarction and a plasma IL-6 concentration above the median at admission had an increased cardiovascular risk, which supports the importance of IL-6 as a risk marker in CHD.
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| 3. |
- Lundman, Pia, et al.
(författare)
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A high-fat meal is accompanied by increased plasma interleukin-6 concentrations
- 2007
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Ingår i: NMCD. Nutrition Metabolism and Cardiovascular Diseases. - : Elsevier BV. - 0939-4753 .- 1590-3729. ; 17:3, s. 195-202
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIM: Enhanced and prolonged postprandial lipaemia is associated with coronary heart disease (CHD). However, the mechanisms linking postprandial lipaemia to the increased risk of atherosclerosis and CHD remain to be determined. The aim of the present study was to examine the effects of a high-fat meal on plasma levels of the pro-inflammatory cytokine interleukin-6 (IL-6) and cellular adhesion molecules in CHD patients and control subjects. METHODS AND RESULTS: Forty-one middle-aged men with premature CHD and 26 healthy male controls were investigated. The plasma triglyceride response to the high-fat meal was significantly greater among cases than controls. The oral fat load induced a twofold increase in plasma concentrations of IL-6, an increase that was similar in CHD patients and control subjects. No changes could be detected in plasma concentrations of cellular adhesion molecules in response to postprandial lipaemia in either CHD patients or control subjects. CONCLUSION: The results of the present study suggest that a high-fat meal affects mechanisms that induce increased inflammatory activity, which is recognised as a key modulator in the development of atherosclerosis and CHD. However, the increased levels of plasma IL-6 appear not to be determined by the magnitude of the postprandial triglyceridaemia.
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